To obtain a more complete knowledge of the action of aldosterone on the renal tubule and to examine a possible mechanism of aldosterone escape, the effect of aldosterone administration on renal kallikrein concentration and on kinin levels will be determined. Aldosterone will be continuously infused into intact, conscious dogs and kallikrein and kinin concentrations will be determined daily along with changes in urinary electrolyte and fluid excretion. The marked increase in adrenal glomerulosa sensitivity to angiotensin II and ACT H after sodium deficiency will be studied to determine the mechanism of the increased sensitivity. Studies will be expanded to include hypophysectomized dogs in an effort to determine the essential unidentified pituitary factor(s) for normal aldosterone metabolism during sodium deficiency.